KRAS mutations are commonly associated with a range of solid tumours and haematological malignancies.1 Initial attempts to drug KRAS proved challenging due to the high affinity of KRAS to GTP and the relative abundance of GDP/GTP in human cellular tissue.2 This led a plethora of efforts to target downstream effectors such as RAF, MEK, PI3K, AKT, mTOR and the combination of these signalling nodes,1–3 but these approaches have not led to registration of a drug or drug combinations in the setting of KRAS mutant (KRASM) cancers. The gene discussed is MAP2K7; the disease is cancer.